Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases.
Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases.
复制标题
心血管疾病中的血管平滑肌细胞表型转换。
DOI：
10.3390/cells11244060
复制
发表时间：
2022-12-15
期刊：
影响因子：
6
通讯作者：
Zhang, Jun-Jie
中科院分区：
文献类型：
--
作者：
Tang, Hao-Yue;Chen, Ai-Qun;Zhang, Huan;Gao, Xiao-Fei;Kong, Xiang-Quan;Zhang, Jun-Jie
关键词：
血管平滑肌细胞(VSMCs)是动脉血管壁中的主要细胞类型，具有收缩表型，在生理条件下维持正常的血管结构和功能。作为对应激或血管损伤的反应，收缩的VSMCs可以转换到分化较少的状态(合成表型)，以获得组织修复的增殖、迁移和合成能力。VSMCs表型转换失衡可导致多种心血管疾病，包括动脉粥样硬化、支架内再狭窄、主动脉瘤和血管钙化。明确调控VSMCs表型转换的分子机制对防治发病率和死亡率高的心血管疾病具有重要意义。然而，尽管心血管研究人员进行了长期的努力，但参与VSMCs表型转换的关键分子机制和信号通路仍未完全阐明。本文就VSMCs表型转换在动脉粥样硬化、支架内再狭窄、主动脉瘤和血管钙化中的最新研究和系统知识作一综述，有助于指导未来的研究，并为相关疾病的预防和治疗提供新的见解。
Vascular smooth muscle cells (VSMCs), the major cell type in the arterial vessel wall, have a contractile phenotype that maintains the normal vessel structure and function under physiological conditions. In response to stress or vascular injury, contractile VSMCs can switch to a less differentiated state (synthetic phenotype) to acquire the proliferative, migratory, and synthetic capabilities for tissue reparation. Imbalances in VSMCs phenotypic switching can result in a variety of cardiovascular diseases, including atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification. It is very important to identify the molecular mechanisms regulating VSMCs phenotypic switching to prevent and treat cardiovascular diseases with high morbidity and mortality. However, the key molecular mechanisms and signaling pathways participating in VSMCs phenotypic switching have still not been fully elucidated despite long-term efforts by cardiovascular researchers. In this review, we provide an updated summary of the recent studies and systematic knowledge of VSMCs phenotypic switching in atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification, which may help guide future research and provide novel insights into the prevention and treatment of related diseases.
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